INVESTIGATIONS

Clinical and laboratory

A typical MI is diagnosed by medical history, initial ECG and confirmed by subsequent serial paths, and further supported by the finding of a movement enzyme. However, in some cases, definitive diagnosis may not be possible, the clinical data may be typical or highly suggestive, in the presence of an ECG and enzyme levels: patients are classified as having a possible or probable AMI. It is likely that some of these patients have undergone a modest extension of MI.

 

The diagnosis of AMI should be considered in men> 35 years and women> 50 years who complain of chest pain in particular that must be modulated by pain due to pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral infringement, esophageal spasm, tenderness of the chest muscles after an injury or after exercise, acute aortic dissection, renal colic, splenic infarction and various gastrointestinal diseases. Patients often confuse pain with indigestion and proper assessment of this symptom may be hampered by a coexisting hiatal hernia, peptic ulcer or gallbladder disease. Despite the pain of the gastritis is commonly relieved by antacids or vomiting, this benefit is usually of short duration or only partial.

 

ECG: The most important diagnostic procedure in patients with suspected AMI and ECG. MI transmural (Q-type attack) the initial ECG is usually diagnostic, because it shows abnormally deep Q waves and ST elevation in leads subtending the damaged area, the ECG may also be significantly altered with ST-segment sottoslivellato and elevation or inverted T wave in the absence of pathological Q waves.

Acute myocardial infarction in the anterior, within a few hours after the onset. Note the important ST-segment elevation in: I, aVL, V4, and V6

 Acute myocardial infarction in the front seat after the first 24 hours. Note that the ST-segment elevation is less acute, note also the appearance of Q waves

Acute myocardial infarction in the previous several days after onset. The significant Q waves and the amputation of R waves persist. The ST segment is now essentially isoelectric.

Infero-posterior myocardial infarction, the recorded trace within a few hours of symptom onset. Note the hyperacute ST-segment elevation in II, III and aVF and reciprocal changes in other leads.
 

Infero-posterior myocardial infarction after the first 24 hours. Note the appearance of significant Q waves in leads II, III and aVF and the reduction of ST-segment elevation in the same branch.

Infero-posterior myocardial infarction several days after onset. The ST segment is isoelectric now. There are pathological Q waves in II, III and aVF, indicating that the myocardial scar persists.

 The appearance of a left bundle branch block from scratch can be a sign of a recent AMI. The immediate execution of a 12-lead ECG is crucial for deciding on therapy (patients with ST elevation benefit of thrombolytic therapy). In the presence of characteristic symptoms, the ECG ST-segment elevation had a specificity of 90% and a sensitivity of 45% for the diagnosis of AMI. Paths repeated in a series showing a gradual evolution towards a stable, closer to normal, or the appearance of pathological Q waves in a few days, tend to confirm the initial hypothesis of an AMI. The non-transmural infarction (non Q-wave infarctions) usually affecting the subendocardial layers or mesomiocardici, are not characterized by the appearance of Q-wave diagnostic ECG changes and commonly produce only varying degrees of ST segment and T wave In some patients, the ECG changes are less dramatic, variable or non-specific and therefore difficult to interpret. However, it is possible to diagnose an AMI when repeated ECGs are normal. A normal ECG in the absence of pain does not exclude the presence of unstable angina can progress to an AMI.

 

Routine blood tests: Routine tests showed abnormalities consistent with tissue necrosis. After about 12 h, the ESR is increased and the WBC is moderately high.

 

The CK-MB, myocardial component of the CK, is detected in the circulation within 6 h after myocardial necrosis. The elevated blood levels persist for 36-48 h. Although small amounts of CK-MB are found in other tissues, the increase in CK MB component with> 40% is diagnostic, when combined with clinical data suggestive of AMI. The routine assay of CK-MB at 6-8 h and q in the first 24 h esluderà or confirm the diagnosis. A normal CK-MB for 24 hours virtually rules out an AMI. The myoglobin, and contractile proteins troponin-T and troponin-I are released into the circulation from the infarcted myocardium. Troponin-T and troponin-I seem to be very sensitive marker of myocardial damage and can replace the analysis of CK-MB when you have to take clinical decisions in patients with chest pain and ECG nondiagnostic. The troponins are released in some patients with unstable angina and reached levels correlate with prognosis (how much higher, the greater the likelihood of future adverse events).

 

Imaging to display an AMI, there are two techniques. Technetium-99m pyrophosphate accumulates in the myocardium that has suffered (3-4 days), recent heart attack. In contrast, thallium-201 is concentrated within the cells of the myocardium by mimicking the K and distributed in direct proportion to blood flow. However, scintigraphy is expensive, time-consuming and involves exposure to radiation, in addition, the information obtained is often only of marginal utility in the diagnosis and treatment of EPI.

 

 Echocardiography may be useful to assess the kinetics of the wall, the presence of a ventricular thrombus, rupture of papillary muscle, rupture of the interventricular septum and the presence of an intracavitary thrombus in patients with anterior infarction type Q. When the diagnosis of AMI is uncertain, the finding of segmental LV wall motion abnormalities by echocardiography can determine that there is myocardial damage allegedly caused by a recent or past MI.

 

Right catheterization: treatment of complications of the EPI (eg., Severe heart failure, hypoxia, hypotension) may benefit from relief of pressure in the right ventricle, pulmonary artery and pulmonary capillary using balloon catheters wedge position (Swan-Ganz). The cardiac output can be determined by the indicator dilution technique.

COMPLICATIONS

COMPLICATIONS OF MI:  

A 'arrhythmia of any kind, occurs in > 90% of patients with myocardial infarction. In an early stage, one can observe bradycardia or ventricular ectopic beats (VEB). The conduction disorders may reflect damage to the sinus node, atrioventricular node conduction and tissue specific. The potentially lethal arrhythmia, which is the main cause of death in the first 72 h, include tachycardia of any origin, fast enough to reduce cardiac output and lower the PA, the second-degree AV block type Mobitz II or third degree ventricular tachycardia (VT) and ventricular fibrillation (VF). The complete heart block with wide QRS (atrial impulses fail to reach the ventricle, the ventricular rate is low) is rare and is usually indicative of a massive heart attack earlier. Complete atrioventricular block with narrow QRS usually indicates a heart attack or lower back. The asystole is uncommon, except for cases in which it appears as a terminal event of progressive left ventricular failure and shock.

                                                VENTRICULAR TACHYCARDIA 

 

 

 

 

                                          VENTRICULAR FIBRILLATION

                                                SECOND DEGREE HEART BLOCK

 

 

The disturbances of the function of the sinus node artery depends on the source of the vase that sprays (ie left or right coronary artery) and the possibility, especially in patients in older age, a previous illness. Sinus bradycardia usually does not have any meaning, unless the heart rate is less than 50 bpm. The persistent sinus tachycardia is usually an ominous sign, often an expression of failure of VS and low cardiac output. However, other causes must be sought (eg., Sepsis, hyperthyroidism).

 

Atrial arrhythmias, including atrial ectopic beats (BEA), atrial fibrillation and flutter (fibrillation less common) are found in approximately 10% of patients with AMI and may be an expression of left ventricular failure or right atrial infarction. Paroxysmal atrial tachycardia is rare and usually occurs in patients who have had previous episodes.

 

Atrial fibrillation that occurs within the first 24 hours is usually transient. Risk factors include age> 70 years, heart failure, a previous AMI, a large anterior infarction, a heart fibrillation, pericarditis, hypokalemia, hypomagnesemia, chronic respiratory disease and hypoxia. Thrombolytic therapy reduces the incidence. Paroxysmal atrial fibrillation applicant is a poor prognostic sign and increases the risk of systemic embolism.

 

In atrioventricular block, reversible changes in atrioventricular conduction, conduction disorders that Mobitz type I with PR prolongation or Wenckebach phenomenon, observed with relative frequency, particularly nell'infarto inferior-diaphragmatic, in which case, they are interested vessels that supply the posterior wall of the LV, which gives branches to the atrioventricular node. These disorders are usually self-limiting. The correct ECG diagnosis of the type of block is important. The progression to complete heart block is unusual, the real block Mobitz type II, with missing beats or atrioventricular block with wide QRS complex and slow, and usually represents an ominous complication of massive anterior infarction.

 

Ventricular arrhythmias are common. The primary VF occurs in the first hours after an AMI. The late PV may be associated with myocardial ischemia continues or delayed and, when associated with hemodynamic instability, is a poor prognostic sign. Ventricular arrhythmias may reflect hypoxia, electrolyte imbalance, or sympathetic hyperactivity.

 

The 'heart failure occurs in about 2 / 3 of patients hospitalized for AMI. It is usually the predominant LV dysfunction with dyspnea, inspiratory crackles at the lung bases and hypoxemia. The clinical signs depend on infarct size, increased LV filling pressure and extent of the reduction in cardiac output. -Indicated in the VS, the Pa _O2 before and after administration of an effective fast-acting diuretic (eg., Furosemide 40 mg IV) may be helpful for diagnosis: reduced Pa _O2 caused by failure of the VS should increase after diuresis. The mortality rate varies in direct proportion to the severity of left ventricular.

 

In 'RV infarction, the clinical signs include high pressure filling of the RV, jugular turgor, no significant pathology of the lung fields and hypotension. ST-segment elevation of 1 mm in the right precordial leads (V _4R) is highly indicative of myocardial VD. The RV myocardial infarction complicating a VS is associated with increased mortality.

The 'hypoxemia that commonly accompanies an AMI is usually secondary to increased left atrial pressure resulting in alteration of ventilation / perfusion ratio in the lung, pulmonary edema in the interstitial phase, collapse of alveoli and increasing the share of the physiological shunt. In patients aged between 50 and 70 years, normal values ​​of Pa _O2 at rest in bed is about 82 ± 5 mm Hg.

The 'hypotension in the course of AMI may be due to the reduction of ventricular filling or loss of contractile force secondary to a massive heart attack. A reduced LV filling is most often the consequence of a reduced venous return, in turn, secondary to hypovolemia, especially in patients receiving diuretic therapy intense, but it may also reflect a myocardial VD. To determine the cause of hypotension, it is sometimes necessary to measure intracardiac pressures by means of transcutaneous balloon floating catheter (Swan-Ganz). If (in the presence of systemic hypotension) the pressure in the left atrium is low, it should run a load test fluid (NaCl 0.9% or 0.45%) are administered 200-400 ml of NaCl in 30 min monitoring the systemic and left atrial PA. If the PA salt with only a modest increase in atrial pressure, the diagnosis of hypovolemia is likely. Alternatively (if you do not measure intracardiac pressures), a rise in BP with the clinical improvement and absence of pulmonary congestion suggests hypovolemia.

 

Cardiogenic shock characterized by hypotension, tachycardia, decreased urine output, confusion, profuse sweating and cold extremities, has a mortality rate of 65%. It is mainly associated with massive infarction in the anterior and the loss of a share> 50% of the left ventricular myocardium functioning.

 

A 'recurrent ischaemia may follow an IMA. Chest pain usually disappears within 12-24 hours of the EPI. Any chest pain or residual following may be a pericarditis, pulmonary embolism or other complications (eg., Pneumonia, gastric disorders or recurrent ischaemia). The recurrent ischaemia is usually accompanied by reversible changes of the T wave and ST segment ECG. The PA can be high. Up to 1 / 3 of patients without chest pain were more likely to have silent ischemia (ECG changes without pain). The evidence of continuous post-AMI ischemia suggests the presence of myocardium at risk.

 

A 'functional insufficiency of the papillary muscle occurs in about 35% of patients. Mitral insufficiency, some of which has permanent scarring caused by a lesion of the papillary muscle or free wall. Auscultation frequently during the first hours of infarction can often enjoy a transient apical systolic murmur, believed linked to ischemia of a papillary muscle that causes a complete failure coaptazione mitral valve leaflets.

 

There are 3 forms of myocardial rupture: that of the papillary muscle, rupture of the interventricular septum and the free wall.

The papillary muscle rupture is often associated with an inferior-posterior infarction, coronary artery occlusion had right. It produces an acute and severe mitral regurgitation is characterized by the sudden appearance of a systolic murmur with thrill intense spike in the presence of pulmonary edema.

Rupture of the interventricular septum, although rare, is 8-10 times more common than papillary muscle rupture. It is characterized by the sudden appearance of an intense systolic murmur with thrill, more medial than the apex along the left sternal border at the level of 3 ^{or-4 or} intercostal space, accompanied by hypotension with or without signs of left ventricular failure. The diagnosis can be confirmed by inserting a balloon catheter for the determination and comparison of O ₂ saturation or Po ₂ of blood samples taken from the right atrium from the RV and the pulmonary artery. A significant increase in the values ​​of Po ₂ in the VD is diagnostic. Doppler Echocardiography is often diagnostic.

The incidence of heart failure increases with age and is higher in women. It is characterized by the sudden collapse of the PA, with momentary persistence of sinus rhythm, and the frequent presence of signs of cardiac tamponade. It is almost always fatal.

 

The pseudoaneurysm is a form of rupture of the LV free wall, where a wall made ​​from aneurysmal thrombus and pericardium prevents extravasation of blood.

 

The 'ventricular aneurysm is common, especially in the presence of a large transmural infarction (more commonly the front) and good function of the myocardium remaining. Aneurysms can form in a few days, weeks or months. Do not undergo rupture, but may be accompanied by recurrent ventricular arrhythmias and low cardiac output. Another risk from ventricular aneurysm is the formation of a mural thrombus and systemic embolization. The suspected diagnosis is derived from the relevant inspection or palpation of precordial movements paradoxes accompanied by persistent ST-segment elevation ECG or a characteristic protrusion of the shadow cardiac chest x-ray. Echocardiography helps to diagnose and detect the presence of a thrombus. The administration of ACE inhibitors during the acute phase of stroke affects the LV remodeling and may reduce the incidence of aneurysms.

 

A 'asinergia ventricle may occur because of the juxtaposition of normal and abnormal myocardium in the course of AMI. An akinetic segment does not contract and does not show the characteristic movement of retraction in systole. Hypokinetic segment has a reduced range of contraction and a partial impairment of systolic retraction. In the case of multiple infarcts, the myocardial hypokinesia has spread and, if dominated by low cardiac output and heart failure with pulmonary congestion, it is called ischemic cardiomyopathy. One segment shows dyskinetic systolic expansion or bulging (paradoxical movement). These alterations can be identified by two-dimensional echocardiography, ventriculography or radionuclide angiography and may contribute to the reduction of ventricular function and exercise tolerance in the long term.

 

The mural thrombosis occurs in approximately 20% of patients with AMI (60% of patients with large anterior infarction). Systemic embolism occurs in approximately 10% of patients with thrombosis of the VS (best diagnosed on echocardiography), the risk is higher in the first 10 days but persists for at least 3 months.

 

Pericarditis can cause a pericardial rub in about 1 / 3 of patients with transmural AMI. The rubbing usually appears 24-96 h after the onset of the EPI. An earlier onset is unusual and suggests the possibility of other diseases (eg., Acute pericarditis), although the hemorrhagic pericarditis may occasionally complicate the early stage of the EPI. Tamponade is rare.

 

Postinfarction syndrome (Dressler syndrome) develops in some patients several days or weeks or even months after the AMI, but in recent years its incidence appears to have decreased. It is characterized by fever, pericarditis with a rub, pericardial effusion, pleuritic pain, pleural effusion, pulmonary infiltrates, and joint pain. It can be difficult to differentiate this condition from a reinfarction or infarct extension, but the cardiac enzymes do not increase significantly. This syndrome may be recurrent.

 

PATHOPHYSIOLOGY OF CORONARY ARTERY DISEASE

ETIOLOGY AND PATHOPHYSIOLOGY:

In greater than 90% of patients with AMI, a blood clot formed sharply, often associated with plaque rupture, occludes the artery (which was previously partially blocked by atherosclerotic plaque), which provides blood to the area damaged. Impaired platelet function induced by alterations in the endothelium of atherosclerotic plaque presumably contributes to the genesis of the thrombus. A spontaneous thrombolysis occurs in about 2 / 3 of patients, so that, after 24 h, thrombotic occlusion is found only in 30% of cases.

 

The IMA is rarely caused by arterial embolism (eg. In the aortic or mitral stenosis, infective endocarditis and endocarditis arrowroot). Cocaine causes a major coronary spasm and individuals who use it may develop angina or AMI induced by cocaine. Angiographic and autopsy studies have shown that cocaine-induced coronary thrombosis may occur on normal coronary arteries or duplicate an existing atheroma.

The IMA is mainly a disease of the VS, although the damage could extend to the right ventricle (RV) or the atria. RV infarction is usually the result of occlusion of right coronary artery or a dominant circumflex artery and is characterized by a high pressure filling of the RV, often with severe tricuspid regurgitation and reduced cardiac output. A degree of RV dysfunction occurs in about half of patients with infero-posterior infarction and causes hemodynamic instability in 10-15% of cases. RV dysfunction should be considered in every patient with acute infero-posterior and elevated jugular venous pressure and hypotension or shock.

 

The heart's ability to continue to maintain the pump function is directly proportional to the size of myocardial injury. The patient died of cardiogenic shock usually have a heart attack, or a combination of myocardial scar and again, which affects 50% of the mass of VS. The earlier heart attacks tend to be larger and have a worse prognosis than the inferior-posterior infarction. They are usually caused by occlusion of the left coronary branches, especially the left anterior descending artery, and inferior-posterior infarcts reflect right coronary artery or occlusion of a dominant circumflex artery.

Transmural infarcts affecting the myocardial wall thickness at all, dall'epicardio endocardium, and is usually characterized by pathological Q wave ECG. The non-transmural or subendocardial infarcts do not extend throughout the ventricular wall and cause only ST-segment abnormalities and T wave Subendocardial infarcts usually involve the inner third of the myocardium, where wall tension is highest and the myocardial blood flow is more vulnerable to circulatory changes. They may also follow prolonged hypotension from any cause. Since the extent of myocardial necrosis through the wall can not be precisely determined clinically, infarcts are more correctly classified as non-Q and Q according to the ECG. The amount of necrotic myocardium can be estimated from the volume and duration of the increase in CK.

SIGNS AND SYMPTOMS:

 

About 2 / 3 of patients experience warning symptoms a few days or weeks before the event, including unstable angina, dyspnea or fatigue. The first symptoms of an AMI is usually the deep visceral pain, retrosternal, described as  oppressive, often radiating to the back, jaw or left arm. The pain has characteristics similar to those of angina pectoris, but usually is more intense, lasting and poorly or only transiently relieved by rest or nitroglycerin. However, pain can be very mild and about 20% of acute heart attacks are silent or not recognized by the patient as a pathological event. Women may have atypical chest discomfort. Elderly patients may complain of dyspnea rather than chest pain of ischemic type. In severe episodes, the patient appears anxious and may experience a feeling of impending doom. You may experience nausea and vomiting, particularly lower in the IM. The symptoms of LV failure, pulmonary edema, shock or significant arrhythmias may dominate the clinical picture.

On clinical examination, the patient is in the grip of an intense pain, are usually restless and anxious, with skin pale, cold and sweaty. Peripheral or central cyanosis may occur. The pulse may be wiry and BP is variable, although most patients initially present some degree of hypertension, unless you are developing cardiogenic shock.

The heart sounds are often a bit 'muffled, almost as a rule the presence of a quarter tone. There may be a mild apical systolic murmur (an expression of dysfunction of the papillary muscle). The importance of rubbing or blowing stronger initial assessment suggests a pre-existing heart disease or another diagnosis. The appearance of a rub in the first hours is unusual and may suggest the diagnosis of acute pericarditis rather than IMA. Pericardial friction, usually evanescent, and are common to two or three days after a heart attack.

HEALTHY LIFE

HEART DISEASES:

Coronary heart disease is the highest cause of death in industrialized countries including the United States. Cardiovascular disease does not seem to diminish as an increasing number of obese adults and children seems to be increasing. Cholesterol seems to be growing more and more people and this includes higher levels of LDL cholesterol. LDL cholesterol is one of the factors that can lead to clogged arteries that can lead to different coronary heart disease. Most people are not concerned about this problem until you have had a stroke, heart attack, or other matter.

People need to come to an agreement on LDL cholesterol and bad cholesterol as it can lead to coronary heart disease. LDL cholesterol is produced by the liver and transported around the body to be used in certain functions. However, high levels of LDL and small LDL particles may cause clogging of the arteries as the wax particles in combination with other substances, can slip into the lining of the arteries and plaque build a fort. This is where the human problem as the accumulation of more starts to accumulate, which some studies have linked since childhood. For this reason it is especially important for children to have a healthy diet low in cholesterol.

There are many solutions for LDL cholesterol with the most used is a change in dietary habits and lifestyle. Fast food has been linked to an increase in people who are obese and less healthy. This is because fast food can contain high amounts of saturated and trans fats and provide less nutritional content. Cholesterol is another product that should be limited and found all the food produced by different animals. For many people, changing diets on selecting foods low in saturated fat, trans fat-free foods, and foods with cholesterol can be very little effect on coronary health. For parents, it is important to help children with proper nutrition and routine health which means less fast food and fried foods and healthier alternatives. Some alternatives include the addition of more fish and poultry diets, adding more fruits and vegetables, and replacement items with trans fat or saturated fat with many alternatives. Its good to add  chicken and fish in 5 to 7 days a week. There are no more trans fat snacks as they have been replaced with healthier alternatives such as trail mix, crackers free and low trans fat-free, and cumulative effects of natural fruit. Every time you buy food from the store, Its better to check the nutrition label to check the contents of fat, sugar, and overall nutritional value.  Changes in lifestyles are giving up smoking and adding daily exercise routine to keep active. This is especially important for children these days are more likely to sit and watch TV, play video games, or use the computer. Parents need to add exercise routine family and encourage children to become more active and tend to stay with them. Adults need to add exercise to their routine as well.

There are many alternative foods that still taste great but are low in saturated fat and no trans fats. There are a lot of options other food joints next to fried fast food. It 'also important to ensure your children grow up healthy and do not put all the blame on fast food to make our children fat. 

REMEDIES AGAINST HYPERTENSION

Two fundamental devices are the 'exercise and a change in' ​​power.

 

And even if your doctor has prescribed a drug to lower blood pressure, these changes in lifestyle are essential.

 

• Weight reduction if overweight or obesity 
• Restriction of alcohol consumption
• Limiting smoking to stop smoking or better. The substances contained in tobacco smoke contribute to harden the arteries, causing damage to blood vessels, while the nicotine in cigarettes causes blood vessels to narrow
• Limit your intake of coffee
• It 'an appropriate restriction of sodium (salt) in 4 / 6 grams per day, achieved by not adding salt in cooking and flavored with garlic, onion, sage, parsley, basil, rosemary, lemon, and avoid processed foods' use of extracts or nuts
• There should be a good supply of calcium (1 gram per day), consuming milk or yogurt and / or low fat dairy
• There should be a good supply of potassium (100 mEq / day), increasing consumption of fresh fruits and vegetables (even frozen). Usually the higher the levels of potassium in the urine and lower the pressure
• Make a 'moderate physical activity (walking, cycling, swimming)
• Practicing any relaxation techniques
• Ensuring a sufficient number of hours of sleep
• Consistently follow the medication prescribed by your doctor
• Regularly check your blood pressure and maintain close contact with your doctor
• Try a little 'peace of mind do: interacting with animals, be it a walk with the dog, petting a cat or just observe a tank with fish, leading to a fall in blood pressure
• Fun hobbies like gardening, or playing a musical instrument eg. embroidery, have beneficial effects
• Do not go around by car when there is too much traffic on the street is well known that driving in heavy traffic causes fatigue and increases the level of stress

In Australia have discovered that a sprinkling of ' garlic (600-900 mg) can help lower blood pressure by 8.4 points systolic pressure (the maximum) and 7.3 points diastolic (lowest).

 

Some experts recommend eating a clove of raw garlic per day.

 

Others suggest a dose of dried garlic equivalent to about 4 g of fresh garlic per day.

 

Also abound with the onions, thanks to their content of quercetin (30/50 mg per pound), for experts from the University of Utah (USA), helps to lower the maximum of 7 points and 5 the least.

 

The omega-3 fats are contrasting blood pressure and reduce the risk of cardiac arrhythmia. According to research reported in the journal Circulation enough 5.6 grams per day of these fats to lower pressure levels of 3.4 points (in a piece of salmon there are contained about 3 grams).

Omega-3 inhibit the body's production of substances such as prostaglandins that narrow arteries.

 

You can also take a tablespoon of flaxseed oil per day, dissolved in juice or added to salad dressing.

 

In addition, the wine can increase levels of omega-3: University of Campobasso have found that two glasses a day, the concentration of omega-3 increases.

 

According to research presented at the meeting in New Orleans of the American Society of Hypertension, just half an hour of music a day lowered by 3 points, the pressure of systolic and diastolic blood pressure 4: there are kinds advice, just listen to the music you love, the authors explain.

 

According to a study published in Nutrition, extracts of green tea reduces the maximum of 5 points and 4 the least and also lowers cholesterol levels.

 

It seems to be useful to take Magnesium : This mineral helps relax the smooth muscle tissue located. The recommended doses for lowering blood pressure are 400 mg of magnesium and 1,000 mg of calcium daily.

 

It seems to work by interfering with the angiotensin converting enzyme (ACE), which narrows blood vessels.

 

This enzyme is targeted by ACE inhibitors, drugs that reduce blood pressure.

In principle, a controlled diet, sporting three sessions a week, two glasses of wine a day, low-stress and zero cigarettes, this is the formula that saves us from hypertension.

BLOOD PRESSURE

If the measurement of your blood pressure indicates high blood pressure, it means that your heart is making more effort than it should to pump blood and your arteries are under pressure.

 

This situation is dangerous.

 

In fact, if you do nothing to lower blood pressure, increases the risk of stroke, heart attack , kidney disease and other deadly diseases.

 

Half the people who suffer from high blood pressure do not know they resent.

 

An examination of the blood pressure is a great protective and preventive measures that we can do to our body, in fact allows for the immediate control of the circulatory system.

 

Many fear that high blood pressure prelude to disability and premature death.

In the circulatory system, the heart and arteries need to maintain a given pressure to push blood through the vessels that go hand in hand shrinking: from the arteries to arterioles and capillaries from these.

 

Without that blood pressure could not feed the billions of hungry cells of the body.

 

Dozens of times a day the pressure is subject to large fluctuations to meet the needs of the organism.

 

Generally, for the blood pressure monitor: inflating the cuff, the doctor pressed against the main artery of the arm bone, to stop the circulation of blood when listening with the stethoscope, hear the heartbeat stop, it begins to deflate slowly the sleeve.

If they finds blood pressure at the instant when the pulse starts to pulsate.

This is the systolic pressure, ie the maximum pressure in the arteries when the heart contracts.By continuing to deflate the cuff, the doctor makes a second reading when the pulse disappears again when the heart, for a small fraction of the time, rest.This is the diastolic pressure, ie the minimum pressure in the arteries between beats and the other of the heart.

Few doctors trust a single test.

 

Many factors can lead to incorrect index of high pressure, even the anxiety caused from the examination itself.

 

Usually we tend to do several tests, taking into account the lower figures.

 

It 's the lower pressure, diastolic blood pressure that can probably affect more than the systolic.

 

In fact reveals the effort which is subject to the heart between beats and the other, when it should take that rest is vital.

 

In a sense you can think of diastolic blood pressure as a measure of quality of rest that is given to the heart.

 

In moments of anger, adrenaline contracts the arteries, causing increased pressure, as in a those when it is pressing in this way the body receives a fresh supply of energy to meet a critical condition.

 

Another controller is the carotid sinus in the neck, a slight swelling main artery that carries blood to the head.

 

When this small bag inflates too much blood, his nerves send a message to the brain, which responds by ordering the muscles of the walls of the arteries to relax and the heart to slow down, thus lowering the pressure.

Blood pressure (mm Hg)	Normal values	Limit values	High Blood Pressure
systolic = higher value	up to 140	141-160	over 160
diastolic = lower value	up to 90	91-95	over 95

 

In 'essential hypertension blood pressure is too high.

 

Some symptoms of hypertension include: chronic headaches, palpitations, shortness of breath, fatigue, nosebleeds, blurred vision, flushed face, frequent urination, ringing in the ears.

Tension and various efforts, constant anxiety and fatigue can contract the artery walls and to increase the pressure, if the force or tension persists, the pressure is maintained at a high level, imposing a burden on the heart and arteries.

Often the heart expands to cope with more work.

The arteries lose their normal elasticity and harden.

If nothing is done, the heart may fail by excessive work, can form a clot that blocks blood or corroded artery can rupture in the brain.

Hypertension, if not corrected, increases the thickness of the heart muscle at risk of heart failure.

Hypertension upsets the structure of the arteries of the heart (with risk of angina and myocardial infarction), brain (risk of stroke), retinal (reduction of vision), kidney (renal failure).

Sometimes the examination of blood pressure gives lower figures than usual.

People often complain of fatigue that are affected but the low blood pressure predisposes to a long and healthy life.

 

No one should fear the cuff to measure pressure, we can even say that is one of our best friends.

There is a curious German research published in the Journal of the American Medical Association which states that the polyphenols in chocolate (dark) help dilate blood vessels.

 

A little more than 6g a day in 4 months have reduced the pressure so that 18% of patients did not suffer more hypertension.

 

By controlling the pressure levels reduces the risk of suffering from arrhythmia.

 

An alarm signal for this kind of problem is the sharp drop in resistance during cardiovascular workouts.

HEART MURMURS

Are sounds produced by turbulent flow generated by the passage of blood in narrow areas (strictures) in hyperdynamic conditions (anemia, thyrotoxicosis, pregnancy, etc.) Blood reflux in incompetent valves, abnormal communications (eg.: septal defect, persistent arterial duct). There are murmurs that are heard in systole and others, in diastole. Although most murmurs represent any organic disorder, there are some, especially in children and young adults, who are considered functional, and no great importance. These are called innocent murmurs which are characterized by occurring in systole, ejection rate are not giving thrills, never occur in diastole and not associated with an organic disorder.
 
Features blows where it should be fixed:

• If it occurs in systole, in diastole, or both phases of the cardiac cycle.
• The moment occurs. Prefixes are used proto, meso and television to describe murmurs that occur mainly at the beginning, middle or end of systole and diastole, respectively (eg midsystolic, if it occurs in half of systole; protodiastolic, if it occurs at the beginning of diastole).
• His relationship with the heart sounds (eg, the murmur of mitral stenosis begins with the opening snap, and the murmur of aortic stenosis, you can start by clicking the aorta, "which is not always audible, and that occurs after the first sound).
• The intensity of sound. To evaluate this aspect, there is a scale of 6 degrees or levels. The intensity of the murmur is expressed as a ratio where the numerator is indicated which corresponds to the breath and the denominator of the full scale value (eg, murmur grade 2 / 6). These intensity levels are:
• Grade I: When it is difficult to hear in a quiet room (even, it is possible that not all reviewers will listen).
• Grade II. Weak, but all the auscultated examiners.
• Grade III. Moderately strong, clearly audible.
• Grade IV. Strong, began to be felt a thrill.
• Grade V. Very strong and thrill.
• Grade VI. Very strong, can be heard even without supporting the diaphragm of the stethoscope on the surface of the chest palpable thrill.
• The shape of the breath:  in decrescendo, holosystolic, continuous.
• The ejection murmur occurring in systole and depend on the pressure gradient generated by the contraction of the myocardium, have a diamond shape: it increases to a maximum and then decrease.
• Regurgitation murmurs of incompetence of atrioventricular valve begins with the noise, remain relatively constant throughout systole and reach the second sound, or even what encompass, are called holosystolic or pansystolic.
• Regurgitant murmurs of aortic valve incompetence or lung, occurs in diastole, beginning immediately after the second noise and decrease in intensity until it disappeared (in decrescendo).
• Murmurs due to stenosis of the mitral or tricuspid valve, occurs in diastole, after opening the valve (opening snap), and decreases in intensity until it disappeared (in decrescendo). If the patient is in sinus rhythm at the end of diastole and immediately before the first noise may be heard a brief crescendo murmur due to atrial contraction (booster presystolic).
• The focus where it listens more intense irradiation.
• If you change with respiration or with some maneuvers such as straining, exercise, push or squatting (eg: a tricuspid regurgitation murmur increases with inspiration more blood to the right cavities).
• The pitch of sound: high, medium, low. The low key blows are heard best with the bell of the stethoscope.
• The ring also may be different, with some rough character, grunts, music, etc.

 
Characteristics of blows, with particular reference to whether they occur on the systole or diastole:

Murmurs that occur in systole:

Mid-systolic murmurs or ejection type:

Murmurs are most frequently found. These are people whose intensity is greater in the middle of systole, and usually end before the second noise (R _2). Its diamond-shaped (crescendo-decrescendo) is not always obvious and the space between the end of the blow and R ₂ helps to differentiate the holosystolic (or pansystolic).

• Innocent murmurs: Are due to the ejection of blood from the left ventricle to the aorta. Occasionally may be generated by right ventricular ejection. Not associated with cardiovascular disease. Are more frequently found in children, young adults and older adults occasionally. Heard in the 2 nd, 3 rd and 4 th intercostal space between the sternum and the apex, are mild and short-irradiation.

• Physiological murmurs: Are due to turbulent flows that originate on a temporary basis and are in anemia, pregnancy, fever, and hyperthyroidism. Closely resemble innocent murmurs. Are identified by the basic condition to which they are associated.

• Aortic ejection murmur: Heard best at the base, especially in the second space parasternal right, but also in the left sternal border and apex. Radiate to the base of the neck. Could hear better with the patient sitting and leaning forward. May be preceded by a click of the valve opening, which is not always heard. Found in aortic stenosis (congenital, rheumatic, degenerative), narrowing the outflow tract (eg hypertrophic cardiomyopathy), dilated distal aorta, or increased flow in systole as in aortic insufficiency. Most murmurs are innocent and physiological aortic ejection rate but try not to associate separate cardiovascular disease. When the murmur is heard best at the apex, you should be careful not to be confused with a murmur of mitral regurgitation.

 

• Pulmonary ejection murmur: Heard best in the 2 nd and 3 ^rd left parasternal space. If it is strong, it can radiate to the left neck. Found in pulmonary valve stenosis (more common in children and cause congenital) and pulmonary hypertension. An increase in flow can also cause this breath, as in an atrial septal defect (in this condition, the mid-systolic murmur is due to increased flow through the pulmonary valve and not the flow through the atrial septal defect).

• Pansystolic or holosystolic murmurs: These are people dealing with the systole, beginning immediately after the first sound (S ₁₎ and continue until the second sound (S _2), maintaining a fairly uniform intensity.

• Murmurs of mitral regurgitation:  Are due to an incompetent valve (mitral regurgitation). Heard best at the apex and radiated to the axilla, occasionally radiating to the left sternal border. Can be heard better in the left semi-lateral decubitus. Not increase with inspiration. On occasions, such as mitral regurgitation due to ruptured chordae, irradiation can occur around the base of the heart and tend to be confused with murmurs of aortic stenosis. The first sound is diminished.

• Murmurs of tricuspid regurgitation: Are heard when the valve is incompetent (tricuspid regurgitation). The most common cause is failure and dilated right ventricle, which may be secondary to pulmonary hypertension, which in turn can lead to left ventricular failure. Are holosystolic murmur that increases with deep inspiration. Are best heard in left lower sternal border. Radiating to the right of the sternum, and perhaps somewhat to the left, but did not radiate to the axilla. Unlike mitral regurgitation in tricuspid regurgitation following occurs:
• The murmur increases with inspiration.
• there is a wave "v" giant in the jugular venous pulse.
• liver could be a heartbeat it's like to feel the bottom edge of the liver (not to be confused with a hepato-jugular reflux is increased jugular venous distension to apply pressure to the edge of the liver that can be seen in congestive pictures) 

• Holosystolic murmur due to a ventricular septal defect (VSD): The manifestations depend on the size of the communication. Whereas an injury that is not associated with other abnormalities, with a short left to right, you can sound out a holosystolic murmur that is high intensity and produces a thrill. The second sound may be obscured by the intensity of the murmur. Heard best in the 3, 4 and 5 left parasternal area, but has extensive irradiation. In diastole, you can hear a third sound or murmur decrescendo.

Murmurs by a prolapse of the mitral valve: Are end-systolic (occurring in the second half of systole) and may be preceded by a mid-systolic click. They are difficult to auscultate. Sometimes found in patients with pectum excavatum.

Murmurs that occur during diastole:

• Murmurs of aortic valve insufficiency: Begin after the second sound and its intensity is in decrescendo and disappear. Are heard at the base, left sternal border and even at the apex. Are best heard with the patient sitting, leaning forward and exhalation, without breathing for a few seconds. Are heard with the stethoscope diaphragm. To recognize it should be noted other manifestations that can occur:
  • pulse speed or water hammer, is a comprehensive and hyperdynamic pulse.
  • other characteristic of water hammer pulse is that if the examiner takes the patient's forearm using surface feel of his fingers over radial pulse area, near the wrist and forearm up from the horizontal position, you will feel the pulse more widely.
  • in the nail bed may notice a beat when you apply light pressure from the edge of nail.
  • head may have a slight oscillation following the pulse rate.
  • noticeable in the neck large beats (dance arterial).
  • arterial pulse pressure is increased (difference between systolic and diastolic) pressure is slightly increased systolic and diastolic presents a significant decline.
  • in the groin area could hear a double blow femoral (systole - diastole).

In the case of a severe leak can cause a rise of anterior leaflet of the mitral valve and cause a functional stenosis able to take a breath and rolled mitral (Austin Flint murmur), which is heard at the apex and towards the armpit, left semi-lateral decubitus. On the effect of aortic reflux on the mitral valve leaflets, preventing maximum aperture, the first noise could be decreased. Another blow that can be generated secondarily by the increased flow rate is for mid-systolic aortic ejection.

• Murmurs and insufficiency of the pulmonary valve: Begin after the second sound and are in decrescendo. Occur in conditions associated with pulmonary hypertension (Graham Steell breath).

• Murmurs of mitral stenosis: Begin with the opening snap. It has two components: an initial decrescendo murmur (mitral shot), which corresponds to the rapid filling phase, and a presystolic reinforcement in crescendo, which is due to atrial contraction, and that is lost when there is atrial fibrillation. Are heard at the apex, especially in the left semi-lateral decubitus with the patient during expiration. Could be heard best with bell of stethoscope. The first sound is more intense . For the congestion that occurs toward the back of the valve, P ₂ is more intense and the split second sound is heard, the right ventricle can become palpable. The arterial pulse is of low amplitude. When the mitral murmur is caused by inflammation of the valve leaflets by an active rheumatic disease called Carey-Coombs.

• Tricuspid stenosis murmurs: Have characteristics similar to what happens in mitral stenosis, but are unlikely to be found. It is better to auscultate tricuspid focus. In an atrial septal defect murmur can be heard with these features by increasing flow through the valve.

Other heart murmurs:

• In a persistent arterial duct: It is a communication between the aorta and pulmonary artery flow increases at the lungs and left heart. You hear a continuous murmur, which covers the systole and most of diastole (machinery murmur). Is more intense toward the second sound, coming to hide. Is heard in the left second intercostal space, below the collarbone, and may be accompanied by a thrill.

• In an atrial septal defect (ASD): Is associated with a left to right shunt. In systole can be listening to a pulmonary ejection systolic murmur and the diastolic one shot by increased flow through the tricuspid valve.

 
 Tricuspid stenosis: Is usually rheumatic in origin and is associated with mitral stenosis is most evident when listening. What would be more characteristic of tricuspid stenosis is an engorgement of the jugular veins, wave "a" giant. The opening snap and diastolic ferries tend to be obscured by the noise equivalent due to mitral stenosis. 




Pulmonary stenosis: Is the heartbeat of the right ventricle is heard sustained a pulmonary ejection systolic murmur. There could be a wave "to" increased in the jugular venous pulse. Could also be listening to a pulmonary ejection click and a splitting of second sound.




Coarctation of the aorta: Is characterized by stenosis usually is after the origin of the subclavian vein. To proximal collateral circulation develops that tends to compensate for the lower distal flow exists. Hypertension was found in the upper extremities and hypotension in the lower, is also perceived difference in pulse amplitude (the small palpable femoral). In the interscapular region can be listening to a late systolic murmur.

Some special maneuvers:
To differentiate the murmur of aortic stenosis with a hypertrophic cardiomyopathy patient is asked to bear down (Valsalva maneuver) so that the amount of blood reaching the left ventricle decreases, the murmur of aortic stenosis and decreases of cardiomyopathy hypertrophic increases. For the same purpose, if the patient is placed in a squatting position, venous return and blood flow to the ventricles increases, the murmur of aortic stenosis increases and decreases of hypertrophic cardiomyopathy.